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1. Rheum RC > OP / Paget / Bone diseases > Flashcards

OP / Paget / Bone diseases Flashcards

1
Q

** Modifiable RF for OP**

A

-Low Ca or vit D
-Sedentary
-Smoking, Caffeine/Alcohol (>2/d)
-Drugs: GC, Lithium, Heparin, AED, Aromatase inhib, Tamoxifen,

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2
Q

** Nonmodifiable RF for OP**

A
  • Age
    -Race (caucasian, asian)
    -Female
    -Early menopause
    -BMD - Slender build
    -Positive family hip # hx
    -Comorbid: RA, hyperPTH, thyroid, hypogonad, celiac, bypass, Freq falls
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3
Q

OP Diagnosis

A

Fragility Fracture = OP

Low BMD:
-T score <-2.5 in pt >50 w/o fracture; OR
-Z score <2 for premenopausal woman or man <50

High Frax: >20% for major OP # or >3% hip #

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4
Q

** OP physical exam findings**

A

-Weight <60kg
-BMI <20
-Height loss 2cm+ prospective, 6cm+ historical

-Rib pelvis <2fingerbreadths
-Wall to occiput >5cm
-Tooth count <20
-Kyphosis
-Arm height span >5cm

-Grip strength
-Hand skinfold thickness

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5
Q

** How to detect vertebral # **
– Clinically
– Investigations

A

Clinically: ht loss 6cm, dorsal kyphosis, occiput to wall, rib to pelvis

-XR (vertebral body height of at least 20% or 4mm height reduction) or DXA

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6
Q

Indications for BMD testing

A
  • > 50 with 2 RF, >65 with 1, >70
    -Estrogen deficiency with 1 RF for OP
    -Vertebral deformity, fracture, or osteopenia on XR
    -Hyperparathyroid
    -Steroids: >5mg x3mo
    -Monitoring response to OP meds
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7
Q

What is Z score and what does it tell you

A

Zscore = adjusted for age
-Tells you if there’s something other than age or menopause causing low BMD

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8
Q

** Low BMD DDx**

A

-Cushings, Hypogonadism, Hyperthyroid/PTH
-RA, SLE, Ank Spond
-Eating/exercise disorder
-Meds, Alcoholism

-Renal failure, RTA, chronic hypoNa, idiopathic hypercalciuria, MM
-IBD, Celiac, PBC, gastrectomy/bypass

-Osteomalacia, osteogenesis imperfecta, ehlers danlos

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9
Q

** Meds causing low BMD **

A

Steroids,
Lithium, SSRI, Antipsychotic
-AEDs,
-Excess synthroid
-Tamoxifen, Aromatase inhib,
-Cyclosporin,
-Chemo,
-Leuprolide,
-Heparin

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10
Q

Low BMD Labs

A
  • Ca, albumin, PO4
    -PTH, TSH
    -Vitamin D
    -Cr
    -ALP
    -Testosterone
    -Urine calcium, Na, Cr
    -SPEP (if >50yo and abnormal CBC)
    -Celiac antibody
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11
Q

RF for freq falls

A

-Frailty, lower extremity disability
-Meds (sedatives)

-Impaired vision and cognition
-Obstacles in the home

-Previous fall

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12
Q

Nonpharm Tx OP

A

Ca
-Vit D
-Stop smoking
-Exercise

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13
Q

** GIOP pathophysiology**

A

-OB: apoptosis and reduced development (decr Wnt)
-Osteocytes: apoptosis (via caspase 3)
-OC: increased due to decreased sex steroid (incr RANKL) and osteoprotegerin (inhib of resorption)
-Ca: increase renal excretion, decrease GI absorption
-Muscle mass decreases (falls risk)

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14
Q

** CAROC components**

A
  • BMD
    -Age
    -Gender

-Previous fragility fracture >40 or prolonged steroids (>7.5mg/d x3mo) (increase risk class by 1)
-Vertebral/hip fracture or >1 fragility # = high risk

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15
Q

** FRAX components**

A
  • Age
  • Sex
  • Previous fragility #
  • BMI
  • Parental hip fracture
  • Rheumatoid arthritis
  • 2ndary conditions that contribute to bone loss (T1DM, osteogenesis imperfecta, untreated hyperthyroid, hypogonad or premature menopause <45 years, chronic malnutrition, malabsorption, chronic liver disease)
  • Current smoking
  • Alcohol intake (3+/day)
  • Femoral neck BMD
  • Country of current living
  • Steroid exposure (current or >5mg x3 mo)
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16
Q

FRAX risk cutoff

A

Low: <10% MOP, <1% hip #
-Med: 10-19% MOP, 1-3% hip #
-High: >20% MOP, >3% hip #

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17
Q

When to treat GIOP

A

Over 40:
-Low risk FRAX + pred 5-7.5mg/d >3mo
-Med risk FRAX + pred >2.5mg/d
-High risk
-
-Under 40:
-Low risk: if >10% BMD loss in 1 yr or expected >5g pred in 1 year
-Medium and high risk

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18
Q

Pregnancy OP Med Considerations

A

Teriparatide if preg anticipated
-Risdedronate (least fetal tox)
-Prolia CONTRAINDICATED

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19
Q

** Vit D metabolism**

A

Skin makes D3 (cholecalciferol) from sun
-Diet intake D2 (ergocalciferol) and D3
-Both converted to 25-OH-vit D in liver
-Converted to 1,25-OH2-Vit D in kidney by 1 alpha hydroxylase (induced by PTH and hypophosphatemia; inhib by fibroblast growth factor 23)

-1,25OH2 vit D binds intestinal vit D receptor for Ca/PO4 absorption

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20
Q

Osteomalacia / Rickets clinical /imaging features

A

Soft bones from impaired mineralization
- Pain/deformity long bones and pelvis
- XR: pseudofractures

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21
Q

Vit D def osteomalacia lab results

A

Low Ca, PO4, Vit D, 24h urine Ca
High PTH and ALP

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22
Q

Renal PO4 wasting osteomalacia labs

A

Low PO4, high urine PO4,
High ALP,
Normal/inappropriately low Vit D for ALP lvls

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23
Q

Rickets congenital causes

A

X-linked Hypophosphatemic → increased FGF23 → phosphaturic and decrease intestinal absorption of vit D

-Congenital 1 alpha hydroxylase def

-Congenital vit D resistance

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24
Q

** Osteomalacia causes**

A

Vit D deficiency:
- Low PO intake, insuff sunlight, malabsorption, pancreatic insuff,
- Liver/renal dz → insuff vit D conversion,
- Drugs (AED, anti TB, HAART)

HypoPO4:
- Low PO intake
- PO4 binding antacid,
- Excess renal loss , Fanconi,

-Hypophosphatasia - from ALP gene mutation =can’t break down PP (inhibitor of mineralization)

Inhibitors of mineralization:
-Bisphosphonate,
-Aluminum,
-Fluoride

Oncogenic osteomalacia
-FGF23 secreting tumor - inhib PO4 transport and 1-a-hydroxylase enzyme in kidney

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25
Q

Rickets manifestations (NOT in osteomalacia)

A

-Widened cranial sutures
-Growth retardation

-XR: widened metaphyses and growth plates, thin cortex, sparse trabeculae

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26
Q

Ricketts/osteomalacia Tx

A

Vit D deficiency/resistance or malabsorption: → Vitamin D

Renal disease, hypophosphatemia, alpha hydroxylase deficiency: → calcitriol and oral PO4

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27
Q

Familial hyperphosphatemic tumoral calcinosis mutation and result

A

Inactivating mutation of FGF23 → painful ectopic calcification and elevated PO4 lvls

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28
Q

Osteogenesis imperfecta cause & Tx

A

Defective osteoblast fcn
-Tx: bisphosphonates in all by Type IV

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29
Q

Hypophosphatasia
-Cause
-Manifestations
-Tx

A

Cause: mutations inactivating alkaline phosphatase

-Manifestations: fetal demise, rickets, osteomalacia, #, OP, low ALP, high vitamin B5, high urine phosphoethanolamine

-Enzyme replacement, asfotase alpha

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30
Q

Osteopetrosis
-Cause
-Manifestations
-Tx

A

Defective osteoclast fcn → chalky fragile bone and osteosclerosis

-XR: generalized osteosclerosis

-Tx: Bone marrow transplant for normal osteoclasts + calcitriol to stimulate OC

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31
Q

** Paget’s pathophysiology**

A

Mutation or paramyxovirus infxn →
-LARGE OVERACTIVE OC → focal areas of excessive resorption(LYTIC phase)

-OB compensate to increase bone → DISORGANIZED weaker bone(MIXED lytic/sclerotic phase)

-Resorbed bone replaced w/ fibrous tissue and abN enlarged sclerotic bone (SCLEROTIC phase)

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32
Q

** Paget’s manifestations**

A

Bone pain (nocturnal, rest/activity)
-Deformities (tibial bowing, skull thickening) → neural compression
-Pseudofractures (transverse, chalkstick)
-Secondary OA

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33
Q

** Paget’s XR findings**

A

-Osteolysis w/ sclerotic changes (eg cotton wool skull, Osteoporosis circumscripta)
-Tam o Shanter sign
-Spine: picture frame sign, vertebral squaring,

-Coarse trabecular pattern
-Bone enlargement, Cortical thickening
-Blade of grass sign (wedge shaped resorption of long bones)
-Pelvic brim sign or Pelvic Ring

-Bowing deformities
-Pseudofractures (transverse linear radiolucency)

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34
Q

Pagets DDX

A

Chronic OM
-SAPHO
-Cancer: Osteosarcoma, vertebral hemangioma, lymphoma, mets (breast/PCa)
-Hyperostosis frontalis interna
-Fibrous dysplasia

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35
Q

Paget’s phases

A

Lytics
-Mixed lytic/sclerotic
-Sclerotic

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36
Q

Paget Dx vs monitoring

A

Dx: XR
-Extent of bone dz = bone scan
-ALP (high during osteoblastic)
-Bone specific ALP (BSAP) if liver dz falsely elevating ALP

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37
Q

Tx Paget

A
  • Ca, Vit D
    -Bisphosphonate (inhib OC): ZA = drug of choice
    -Prolia (not approved indication)

-NSAID
-If neuropathic pain: gabapentin, pregabalin, amitriptyline

-Ortho consult: bone deformities, spinal canal stenosis, pseudofractures

-Canes, shoe lifts

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38
Q

Paget when to treat

A

-Symptoms: bone pain, radiculopathy, paraplegia, neural impingement, tinnitus, CHF, hearing deficit, H/A

-High risk sites: skull, spine, near major joints

-Pre-surgery near pagetic site (vascularity → blood loss)

-Hypercalcemia assoc’d w/ immobilization

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39
Q

**Paget complications categories **

A

MSK
-Neuro
-Vascular
-Cardiac
-Cancer
-Metabolic

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40
Q

Paget MSK complications

A

Bone pain,
-Deformities (bowing/bossing),
-Fractures

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41
Q

** Paget Neuro complications**

A
  • Nerve entrapment (spinal nerves, cranial nerves)
  • Deafness (auditory nerve)
    -H/A,Vertigo,Tinnitus,
    -Stroke (blood vessel compression)
  • Basilar invagination
  • Spinal stenosis
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42
Q

Paget Vascular complications

A

-Vascular steal syndrome (carotid blood flow to skull at brain’s expense)
-Hyperthermia

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43
Q

Paget Cardiac complications

A

High output CHF,
-HTN,
-Cardiomegaly,
-Angina

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44
Q

Paget Cancer complications

A

Fibrosarcoma,
-Giant cell tumor,
-Osteosarcoma

45
Q

Paget Metabolic complications

A

TOO MUCH CALCIUM (blood, urine, kidneys)

-Hypercalcemia,
-Hypercalciuria,
-Nephrocalcinosis

46
Q

Bisphosphonate side fx

A

Osteonecrosis (esp in Ca and invasive dental procedure)
-AFF
-Nephrotox
-HypoCa
-Esophagitis, GERD
-Flu like illness
- Uveitis, keratitis, optic neuritis, orbital swelling

47
Q

Bisphosphonate mech of action

A
  • Pyrophosphate analog binds hydroxyapatite on bone
  • Blocks farnesyl pyrophosphate synthase → prevent “ruffled border” formation and ability of OC to adhere to bone
  • Also promote OC apoptosis
48
Q

Prolia mech of action

A
  • Human mAb against RANKL
  • Prevents RANKL and RANK-receptor binding → inhib OC formation and resorption
49
Q

Teriparatide mech of action

A
  • PTH analog binding type 1 PTH R
    -Increases GI and renal reabsorption of Ca
    -Stimulates OB differentiation and survival
50
Q

Romosozumab mech of action

A
  • Humanized monoclonal AB (IgG2)
  • Blocks sclerostin (usually inhib Wnt/Beta catenin signaling pathway)
  • Thus more bone formation and less resorption
51
Q

AFF pathophys

A

BP inhib OC and decrease remodelling → microdamage and stress fracture

52
Q

AFF RF

A

-Small (low height/weight) asian female
-Steroids
-Long term bisphosphonate
-Low bone turnover marker (ALP)

53
Q

AFF manifestations

A

Thigh pain
-Bird beak on lateral aspect
-Stress fracture

54
Q

AFF Ix

A

-XR bilateral femurs - transverse/oblique#, thickened cortex, periosteal elevation, beaking of lateral cortex

-MRI/bone scan

55
Q

AFF Tx

A

-Stop bisphosphonate
-Limited weightbearing
-Surgery: intramedullary nailing
-Teriparatide

56
Q

Differentiate Paget bone pain vs OA

A

Lidocaine injection: helps OA not Paget
-Bisphosphonate: helps paget not OA

57
Q

** Artifactual causes of higher BMD**

A

– OA
– DISH, AS
– Vertebral #

– Thalassemia
– Vascular calcification
– Abdo abscess
– Gallstones, Kidney stones

– Implants: silicone, surgical metalwork, pacemakers, catheters, bullets
– Vertebroplasty and kyphoplasty

58
Q

** True causes of higher BMD**

A

-SAPHO
-Chronic infective OM
-Acromegaly
-Osteopetrosis
-Tumors, Osteoblastoma, Mets (PCa)
-Hep C assoc’d osteosclerosis
-Myelofibrosis, Myelosclerosis, Mastocytosis
-Sclerosteosis
-Pagets

59
Q

At risk areas for AVN

A

-Femoral/Humeral head
-Proximal tibia

-Carpal bones (scaphoid, lunate)
-Tarsal navicular, talus
-Metatarsals

-Vertebral body

60
Q

AVN etiology and causes

A

Disruption of arterial blood supply
– Trauma (hip dislocation, #, surgery)
– Hypercoagulable: SS, Hgbopathy, thrombophilia, coagulopathy, fat emboli, SLE, APLA
– BM hypertrophy/infiltration (Gaucher’s, leukemia, myeloproliferative d/o, STEROIDS)
– BM tox/death (chemo, rads, thermal injury)
– Peds: Legg calve perthes, slipped capital femoral epiphysis
– DM, cushings, pancreatitis, OCP,
– Cancer
– Alcohol, Smoking
– Idiopathic
– Meds: Protease inhibitor for HIV, bisphosphonate

61
Q

Risk factors for jaw osteonecrosis

A

-Age >65
-DM
-Smoking
-Steroid use
-Poor oral hygiene
-Invasive dental procedure (extraction,implants)
-High dose antiresorptive (bisphosphonate or prolia; NOT anabolics)

62
Q

Preventing jaw osteonecrosis

A

Oral exam before starting BP
-Continue BP through dental if 4y and no RF
-Hold if >4y or concomitant steroids

63
Q

** GC fx on AVN **

A

Indirect fx causing ischemia, 2/2:
– Decreased angiogenesis
– Vasoactive amine production
– Increased intraosseous pressure from BM fat hypertrophy

PLUS

Same as GIOP (sex steroids, OPG, OB and osteocyte apoptosis, fx on OC)

64
Q

** AVN XR finding stages**

A

0/1 = Normal
2: Osteopenia, cysts (resorption), sclerosis (repair)
3 Subchondral collapse (“crescent sign” w/o articular surface flattening
4 Flattening of articular surface w/o joint space narrowing
5 Flattening of articular surface w/ joint space narrowing and/or acetabular involvement
6 Advanced degenerative changes

65
Q

AVN MRI findings

A

Line of decreased signal on both T1 and T2

66
Q

AVN bone scan findings

A

Donut sign: Cold spot (AVN) surrounded by “hot area”

67
Q

AVN Tx

A

D/C weight bearing x4-8wks
Taper GCs
Analgesia

If reversible (stage 2 or less) → surgery:
– Core decompression
– Vascularized fibula grafting
– Autologous mesenchymal stem cell injxn

Nonreversible (stage 5-6):
–THA

68
Q

Bone marrow edema syndrome (aka transient osteoporosis of the hip) manifestations

A

Hip pain
-XR= osteopenia
-MRI = bone marrow edema of femoral head AND neck

69
Q

Bone marrow edema syndrome Tx

A

Bisphosphonate
-Analgesia
-Protective weight bearing
-
-NO CORE DECOMPRESSION

70
Q

Diff between BMES on MRI and AVN

A

BMES involves femoral head AND femoral neck

71
Q

HPOA clinical findings

A

-Clubbing

-Skin hypertrophy (pachyderma)
-Coarse facial features

Glandular enlargement:
-Dandruff
-Hyperhidrosis

72
Q

**HPOA XR and synovial fluid **

A
  • Periostitis and Periostosis (bone deposition on periosteum) of tubular bones
  • Acroosteolysis
    -Noninflammatory synovial fluid
73
Q

HPOA secondary causes

A

Lung:
- Cancer (SCC, NSCLC), mets, pleural fibroma
- Cystic fibrosis
- Chronic lung infections, lung abscess
- Mesothelioma
- Bronchiectasis

GI :
-IBD, celiac, PBC
- Cancer: hepatic, GI, POEMS
- HCC, Cirrhosis,
- Whipple,

Other associated:
- Chronic infection - lung, endocarditis, HIV
- Cyanotic congenital heart disease
- Grave’s disease
- Drugs: voriconazole

74
Q

** Give 4 different approaches to minimize GIOP **

A

Weight bearing exercise

-Vitamin D 1000U/d
-Calcium 1200mgd
-Bisphosphonate

-BMD at baseline then q1-2 until off
-Use lowest dose of GC possible

75
Q

** OP Pathophys - Pro and Anti bone formation players**

A

Interruption of normal homeostasis of bone turnover causing deterioration of microarchitecture, low bone mass, and fragility fracture risk

Anti-bone formation: RANKL, MCSF, Frz, Sclerostin, DKK-1, continuous PTH

Pro-bone formation: OPG, Wnt, LRP5/6, B Catenin, estrogen/SERM, intermittent PTH

76
Q

Role of RANKL, OPG , Wnt/B catenin

A

RANKL on OB/activated T cells bind RANK on OC precursors to cause OC differentiation/activation.
- Stimulated by steroids, vit D, OTH, IL1/7/17, TNFa

OPG (cytokine secreted by OB) competitively bind RANKL to prevent RANK binding

Wnt/B-catenin stimulates osteoblasts.
- Frz protein binds/neutralizes Wnt
- Sclerostin & Dickkopf proteins (produced by osteocytes) and block Wnt and OPG

77
Q

** Effect of estrogen on osteoporosis or MoA of SERM/HRT*

A

Binds E2-R to produce OPG competes w/ RANKL for RANK binding –> less OC differentiation

Inhib Sclerostin (usually inhibits Wnt for OB differentiation)

78
Q

** List 4 zones of cartilage and describe the organization of collagen in each.**

A
  1. Superficial - thin collagen fibers parallel to subchondral bone
  2. Middle zone -collagen fibers = radial bundles.
  3. Deep zone - largest collagen fibers perpendicular to subchondral bone.
  4. Calcified zone - collagen fibers penetrate and anchor cartilage to bone
79
Q

** What is the role of RANKL in periarticular osteopenia in RA. Name cells which express RANKL in the joint. **

A

OB and T cells express RANKL

Periarticular osteopenia 2/2 local production of PGE2, TNFa, IL1 causing increase in RANKL

80
Q

** What is the role of anti TNF in bone formation?**

A

TNF increases DKK1 and RANKL to inhibit WNT (osteoblastogenesis) and induces osteoclastogenesis

Theory that TNF decreases bone formation, so TNFi may increased damage in Ank Spond is unsubstantiated.

81
Q

** Calcitriol or vit D mech of action in OP**

A

Physiologic levels
- Binds vitamin D receptor on OB to stimulate RANKL (OC differentation) to release Ca from bone to blood
- In bowel, interaction causes Ca-binding protein expression to promote Ca absorption from gut

Pharmacologic levels
- Inhib bone resorption at higher rate than bone formation

82
Q

** Discuss the role of Vit D other than its role in the skeletal system?**

A

Parathyroid: vit D prevents parathyroid hyperplasia

Heart: deficiency can cause CVD and cardiomyopathy

Immunity: Decreases DC maturation and activation of T cells

Diabetes: vit D deficiency assocd w/ insulin resistance

Cancer: block cell cycle, repair DNA damage, inhib mets, induce apoptosis,

83
Q

** Hormones of bone metabolism **

A

Ca regulating hormones: PTH, calcitriol, calcitonin

Sex hormones: estrogen

Systemic hormones: GH, Insulin like growth factor, Thryoid hormone, Cortisol

84
Q

** Hormones of bone metabolism: PTH
-Site and mechanism of action**

A

Acts on kidney to conserve Ca and stimulate calcitriol production
Increases intestinal absorption of Ca
Increase release of Ca from bone to blood

85
Q

** Hormones of bone metabolism: Calcitriol (active vitamin D)
-Site and mechanism of action**

A

-Increase intestinal absorption of Ca and PO4
-Also acts at kidney and bone level to increase Ca levels

86
Q

** Hormones of bone metabolism: Calcitonin
-Site and mechanism of action**

A

Produced by thyroid to DECREASE Ca lvls:

  • Decreases renal reabsorption of Ca and PO4
  • Transiently inactivate OC to prevent resorption
87
Q

** Hormones of bone metabolism: Testosterone
-Site and mechanism of action**

A

Converted to estrogen in fat cells

88
Q

WHO Definition of normal BMD, vs osteopenia, vs OP

A

Normal BMD if T score >-1
Osteopenia if T score between -1 and -2.4
OP if T score -2.5 or less

89
Q

** Entry criteria for FRAX **

A

Drug naiive patients
>40 yo
Osteopenia on BMD
NO fragility #

90
Q

** Osteoporosis of the hip:
3 metabolic causes?
3 structural causes? **

A

Metabolic cause
- Primary hyperparathyroidism
- Hyperthyroidism
- CKD
- Estrogen deficiency

Structural cause
- Immobilization (eg. astronauts, spinal cord injury, hemiplegia)
- Transient osteoporosis of the hip
- RA affecting hip joint leading to relative disuse

91
Q

**Who should be screened for OP? **

A

Postmenopausal females & males 50-64 w/ previous # or ≥2 RF
Age 65-69 if 1 RF
Age ≥70 if NO RF

92
Q

** Definition of fragility fracture **

A

Fracture sustained from force similar to a fall from a standing position or less that would not have occurred in healthy bone, (excludes skull, C spine, face, hands, knees, feet, ankles)

93
Q

How much calcium and vitamin D supplementation is recommended for a 70-year-old Canadian woman?

A

-Vitamin D 400U/d + vitamin D rich foods
-Calcium 1000mg (1200mg for F) /d from diet

94
Q

Risk factors for vitamin D insufficiency

A
  • Malabsorption: IBD, celiac, bariatric/ gastrectomy
  • Reduced skin synthesis (e.g. limited sun, skin pigmentation)
  • Liver failure/cirrhosis
  • CKD, Nephrotic syndrome
  • Meds affecting vit D metab (AED, GC, HAART)
  • Hypo/HyperPTH
95
Q

** Pros/Cons SERM (eg raloxifene) over HRT? **

A

PRO
- LESS risk of invasive breast cancer, endometrial Ca, or cardiovascular event

Cons
- Only works in vertebral #
- Increased VTE

96
Q

**Pros/Cons conventional HRT over raloxifene? **

A

PROS
- More potent anti-resorptive than raloxifene
- Reduction in hip fracture
- Treats vasomotor symptoms of menopause (raloxifene can cause hot flashes)

Cons
- Concern for CVD and endometrial cancer

97
Q

Indications for PTH treatment

A

aka Teriparatide

  • Post-menopausal women with very high fracture risk, particularly those with vertebral fractures
  • Severe OP T score <-3.5 w/o # or <2.5+fragility #
  • Unable to tolerate BP or failed other therapies
  • AFF
  • Pregnancy
  • Glucocorticoid-induced osteoporosis
98
Q

** Bone markers of formation & loss **

A

Formation
- ALP,
- Osteocalcin,
- P1NP

Loss
- Serum C-telopeptides (CTX)
- Urine or serum N-telopeptides (NTX)

99
Q

Utility of following bone markers

A

1) Monitor adherence or Tx response
2) Secondary causes of OP
3) Predict who will benefit from rx
4) Surrogate for fractures in clinical trials

100
Q

** GIOP when does it occur and Tx**

A

Within 3-6mo (peak in 1st 3mo) with ongoing loss per year after
Tx: BP, Ca, vit D for duration of GC

101
Q

**AFF DDX **

A

Meralgia paresthetica,
GT bursitis,
Hip OA,
AVN,
Bone met

102
Q

What are the risk factors for osteoporosis in AS?

A

OP RF:
- Female,
- Age,
- Post menopausal
- Low BMI,
- Prednisone

Inflammation:
- Disease duration,
- High BASMI
- High ESR/CRP
- Syndesmophytes

103
Q

** Romosozumab black box warning **

A

Increased risk of MI, stroke, CVD (EVENITY)

104
Q

** Dose of bisphosphonates for OP vs Paget**

A

Preventing OP:
Zoledronic acid 5mg yearly (treatment or GIOP) or q2y (prevention)
Alendronate 35mg weekly or 5mg daily (double it if GIOP or treating OP )
Risedronate 35mg weekly or 5mg daily

Paget:
Zoledronic acid 5mg once (can repeat if relapse)
Alendronate 40mg daily x6mo
Risedronate 30mg daily x2mo

105
Q

** Periostitis DDX**

A
  • Infection: osteomyelitis, syphilis
  • Malignancy: HPOA, Leukemia, lymphoma, Langerhans cell histiocytosis, bone Ca, mets
  • Inflammatory: Psoriatic arthritis, reactive arthritis, vasculitis
  • Metabolic: thyroid acropachy, acromegaly, scurvy, vitamin A or fluoride toxicity
  • Drug: voriconazole
  • Other: venous insufficiency
106
Q

** Acroosteolysis DDX **

A

HPOA
Hyperparathyroidism
Psoriatic arthritis
Scleroderma

107
Q

** Differential for sclerosis/collapse of a single vertebral body.**

A
  • Trauma
  • Infection (OM)
  • Cancer - primary, mets, leukemia
  • Osteoporosis
  • Osteomalacia
  • Paget’s disease
  • Hyperparathyroid (OFC)
  • Osteogenesis imperfecta
108
Q

** Differential diagnosis for erosion/dissolution of the clavicle.**

A

Bilateral:
- HyperPTH (acromion is normal, but SC joint may be affected)
- RA (outer 3rd of clavicle affected, later on may affect the acromion)
- Psoriatic arthritis
- Scleroderma
- Atraumatic osteolysis (i.e. weightlifters shoulder from repetitive trauma)
- Osteopetrosis
- Genetic conditions

Unilateral:
- RA
- Post-traumatic osteolysis
- Cancer: myeloma, mets
- Osteomyelitis

1. Rheum RC (23 decks)

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